抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Jeffrey L. Anderson, MD, FACC, FAHA, Chair 

Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect 

Nancy M. Albert, PhD, RN, FAHA

Biykem Bozkurt, MD, PhD, FACC, FAHA

Ralph G. Brindis, MD, MPH, MACC

Mark A. Creager, MD, FACC, FAHA[#][1]

Lesley H. Curtis, PhD, FAHA

David DeMets, PhD[#][1]

Robert A

/pdf/2014-aha-acc-hrs-guideline-for-the-management-of-patients-1v8ficsqox.pdf

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society

The Task Force for the management of atrial fibrillation of the European Society of Cardiology (ESC)  

Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC  

Endorsed by the European Stroke Organisation (ESO)

/pdf/2016-esc-guidelines-for-the-management-of-atrial-ba0601yb9m.pdf

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

/pdf/2016-esc-guidelines-for-the-management-of-atrial-36b2cidm1x.pdf

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS: The Task Force for the management of atrial fibrillation of the European Society of Cardiology (ESC). Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Endorsed by the European Stroke Organisation (ESO)

Supplementary Table 9, column 'Edoxaban', row 'eGFR category', '95 mL/min' (page 15). The cell should be coloured green instead of yellow. It should also read "60 mg"instead of "60 mg (use with caution in 'supranormal' renal function)."In the above-indicated cell, a footnote has also been added to state: "Edoxaban should be used in patients with high creatinine clearance only after a careful evaluation of the individual thromboembolic and bleeding risk."Supplementary Table 9, column 'Edoxaban', row 'Dose reduction in selected patients' (page 16). The cell should read "Edoxaban 60 mg reduced to 30 mg once daily if any of the following: creatinine clearance 15-50 mL/min, body weight <60 kg, concomitant use of dronedarone, erythromycin, ciclosporine or ketokonazole"instead of "Edoxaban 60 mg reduced to 30 mg once daily, and edoxaban 30 mg reduced to 15mg once daily, if any of the following: creatinine clearance of 30-50 mL/min, body weight <60 kg, concomitant us of verapamil or quinidine or dronedarone."

/pdf/2020-esc-guidelines-for-the-diagnosis-and-management-of-38dpic1xu8.pdf

2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS).

To support scientific exchange and activity in the field of cardiac cellular electrophysiology, the German Cardiac Society Working Group on Cellular Electrophysiology (AG 18) established a two-day symposium to be held every 2 years. The second Ion Channel Symposium entitled “Gottingen Channels 2017—Of Benches and Beds” took place in Gottingen from September 22nd to 23rd under the auspices of the German Cardiac Society. A group of national and international experts presented scientific advances in cardiac electrophysiology and rhythmology. The symposium’s primary focus was the significance of cellular electrophysiology findings for the optimization of diagnostic and therapeutic strategies against cardiac arrhythmias. To this end, speakers, chairpersons and attendees discussed the contribution of specific molecular alterations to the initiation and perpetuation of atrial and ventricular arrhythmias. Furthermore, the meeting highlighted how discoveries in electrophysiological research may lead to novel therapeutic targets. The interdisciplinary assessment of mechanisms and therapeutic strategies of cardiac arrhythmias represented a key feature of the meeting. A unique combination of topics and speakers representing both basic science and clinical electrophysiology ensured the scientific success of the “Gottingen Channels 2017” symposium. The next Ion Channel Symposium is planned to be hosted by the incoming co-chair of the German Cardiac Society Working Group on Cellular Electrophysiology in fall 2019.

Report on the Ion Channel Symposium : Organized by the German Cardiac Society Working Group on Cellular Electrophysiology (AG 18).

Drug-drug interactions (DDI) represent a significant problem in modern medicine. The number of patients with multi-morbidity, who take multiple drugs, is constantly increasing (polypharmacy). The related exponential increase in potential DDI is almost incomprehensible. In this article, we review pharmacodynamic DDI and provide clinically relevant examples. In addition, we extensively review pharmakokinetic DDI (e. g. through the cytochrome P450-system or p-glycoproteins) that can modify the plasma concentration of many compounds, thereby also increasing the likelihood of unwanted side effects. Finally we provide tools, which may help clinicians in their daily practice to identify and avoid potential DDI. In the context of an ageing society receiving polypharmacy, a better awareness of DDI and of strategies to prevent them is expected to reduce mortality and morbidity.

/pdf/arzneimittelinteraktionen-die-man-kennen-muss-2hqjki2h3g.pdf

Arzneimittelinteraktionen, die man kennen muss!

Abstract 13977: Mechanisms Underlying Delayed Afterdepolarisations and Triggered Activity in Human Atrial Fibrillation

Introduction: Atrial Fibrillation (AF) is favored by Angiotensin II (Ang II) and reactive oxygen species (ROS), but the mechanism is unknown. We hypothesized that Ang II causes oxidative activation...

Niels Voigt

Papers

Report on the Ion Channel Symposium : Organized by the German Cardiac Society Working Group on Cellular Electrophysiology (AG 18).

Arzneimittelinteraktionen, die man kennen muss!

Abstract 13977: Mechanisms Underlying Delayed Afterdepolarisations and Triggered Activity in Human Atrial Fibrillation

Abstract 14037: Angiotensin II Promotes Atrial Fibrillation in Mice by CaMKII Oxidation

with mitral stenosis MicroRNA expression signature in atrial fibrillation